Published online Jul 7, 2017. doi: 10.3748/wjg.v23.i25.4644
Peer-review started: January 10, 2017
First decision: February 23, 2017
Revised: March 8, 2017
Accepted: April 12, 2017
Article in press: April 12, 2017
Published online: July 7, 2017
Processing time: 179 Days and 1.4 Hours
To evaluate the anti-apoptotic effect of banhasasim-tang (BHSST) on chronic acid reflux esophagitis (CARE) using a rat model.
A surgically-induced CARE model was established in Sprague-Dawley rats. The modeled rats were divided into a treatment group or untreated group, and given BHSST (1 g/kg body weight per day) or water, respectively, for 15 consecutive days (n = 7 each group). Changes in expression of proteins related to nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and apoptosis were assessed by western blotting. Changes in esophageal pathology were analyzed by gross and histological examinations.
The CARE exposure modeled rats showed increased levels of the NADPH oxidase subunit, NOX4 and p47phox in the esophagus. The BHSST treatment completely resolved these CARE-related increases. The CARE rats also showed markers of cytokine stress, including elevated levels of TNF-α and reactive oxygen species as well as of the consequent increase in JNK activation, and subsequent decrease in pro-survival gene expression, such as of Bcl-2. BHSST treatment resolved the CARE-related changes. BHSST also exerted an anti-apoptotic effect, as evidenced by altered expression of the apoptosis-related genes for bax, cytochrome c, and caspase 3. Finally, the BHSST treatment markedly ameliorated the CARE-related esophageal mucosal ulcerations.
In the rat model of CARE, BHSST can suppress development of esophageal mucosal ulceration via regulation of reactive oxygen species-dependent apoptosis.
Core tip: Banhasasim-tang (BHSST) has been used widely as an herbal prescription in East Asia for its therapeutic effects on symptoms associated with gastroesophageal reflux disease. In this study, BHSST is shown to play a protective role against chronic acid reflux esophagitis-induced esophageal mucosal ulcer in a rat model, and that this effect involves regulation of reactive oxygen species-dependent apoptosis.